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Exposure to inflammatory cytokines induces methylation-dependent silencing of FBXW2, establishing an inflammatory memory that preserves DDR1 stability, enabling sustained ligand-triggered receptor oligomerization and downstream NF-\u03baB-NRF2 signaling even in PDAC restrictive stromal environments. Together, these findings identify regulated receptor turnover as a mechanism through which stromal architecture, metabolic state, and inflammatory memory are integrated to control PDAC progression.<\/jats:p>","DOI":"10.1073\/pnas.2616901123","type":"journal-article","created":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T16:12:31Z","timestamp":1790093551000},"update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":0,"title":["Inflammatory memory inactivates AMPK-stimulated DDR1 degradation to enable pancreatic cancer growth"],"prefix":"10.1073","volume":"123","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6253-4081","authenticated-orcid":false,"given":"Fei","family":"Yang","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/013q1eq08","id-type":"ROR","asserted-by":"publisher"}],"name":"Institutes of Biomedical Sciences, Department of Hepatobiliary Surgery and Liver Transplantation, Liver Cancer Institute, Zhongshan 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